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. Author manuscript; available in PMC: 2011 Sep 15.
Published in final edited form as: Cancer Res. 2010 Aug 31;70(18):7155–7165. doi: 10.1158/0008-5472.CAN-10-0668

Figure 1. Loss of BRCA1 correlates with cisplatin sensitivity in murine and human ovarian carcinoma cells.

Figure 1

(A) Schema for murine ovarian carcinoma models. Primary ovarian epithelial cells of the indicated genotypes were targeted with RCAS retroviruses as shown, leading to tumor formation in vivo. See text for details. Each of the six cell lines listed at right was derived independently. (B) Increased cisplatin sensitivity is consistently observed in BRCA1-deficient (TBR) versus wild-type (T) ovarian carcinoma lines. Quantitative dose-response (MTT) assay was performed 72 hours post cisplatin treatment. (C) BRCA1 reconsitution induces cisplatin resistance in human ovarian carcinoma cells. BRCA1-deficient UWB1.289 cells were reconstituted with the control vector or BRCA1 followed by MTT assay at 72 hours. Error bars show SD for triplicate samples. (D) Apoptotic death induced by cisplatin (1μM, 72 hours) in BRCA1-deficient cells, shown by immunoblot for cleaved PARP-1; beta-tubulin (β-Tub) loading control.

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